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Muscle and motor control worksheet
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When we look into the belly of a muscle, we find parallel muscle fibres about 0.1 mm in
diameter, and inside each of these we find several smaller units called fibrils. Inside the
fibrils, the components that actually generate the force are the thick and thin filaments; thick
filaments are made of the protein myosin, and thin filaments mostly of the protein actin.
When the muscle contracts, thick and thin filaments slide over each other. The stimulus that
induces them to slide is calcium, released from the sarcoplasmic reticulum. The thick
filaments bind to the thin filaments, forming structures called cross bridges at the points of
contact.
The point of contact between nerves and muscles is called the neuromuscular junction. Here
a neurotransmitter is released, which is called acetylcholine (or ACh for short). The
neurotransmitter is stored in vesicles at the nerve ending, and these fuse with the nerve
membrane to release their contents into the synaptic cleft. In the postsynaptic membrane,
which in the case of the neuromuscular junction is the membrane of the muscle cell, the
neurotransmitter binds to molecules called receptors which initiate the action potential. To
end muscle contraction, the neurotransmitter is broken down by an enzyme called
acetylcholinesterase.
A motor unit is the smallest part of a muscle that can be independently controlled is the group
of muscle fibres connected to one motor nerve fibre. It consists of a single motor nerve fibre,
together with the group of muscle fibres that it controls.
Motor units are of several types and can be grouped into two broad groups named fast and
slow based on their rate of contraction. Their characteristics are:
Fast:
Strength of contraction (large)
Susceptibility to fatigue (susceptible)
Metabolism (mostly anaerobic)
Found in larger numbers in which kind of athlete (sprinter)
Slow:
Strength of contraction (small)
Susceptibility to fatigue (resistant)
Metabolism (mostly aerobic)
Found in larger numbers in which kind of athlete (marathon runner)
Aerobic metabolism is a very efficient way of converting glucose into energy in the form of
ATP. It generates 36 molecules of ATP per molecule of glucose, compared to only 2 in the
case of anaerobic metabolism. Aerobic metabolism takes place in organelles called
mitochondria. The waste product of aerobic metabolism, carbon dioxide, is removed quickly
from the muscle in the circulation; the main waste product of anaerobic metabolism, lactic
acid, remains in the muscle and this leads to pain because it lowers the pH (low pH is a strong
stimulus for some nociceptors; see lecture 3).
We control the force generated by a muscle in two ways. Firstly, we can vary the number of
motor units that are active. Each motor unit adds an increment of force to the total muscle
force. The other way that we control muscle force is by varying the frequency of action
potentials. If this is low, i.e. there is a long gap between action potentials, the motor unit can
relax completely between “twitch” contractions and not much force is generated. When action
potentials become more frequent, so that relaxation between them is incomplete, the
“twitches” start to add. At very high rates of activation, the fusion of twitches leads to a state
called tetanus, not to be confused with the disease of the same name.
The simplest movements are reflexes, and the simplest of these is the knee jerk reflex; it can
be elicited by tapping on the patellar ligament, just below the kneecap. The afferent (sensory)
arm of this begins with the sensory receptor in the quadriceps muscle that detects stretch of
the muscle, which is called the muscle spindle. The sensory axon arrives in the spinal cord
and makes a synapse with a motor neurone which returns to the same muscle. Activation of
the muscle stretch receptors thus causes the muscle to contract.
Another reflex, with a protective function, involves the Golgi tendon organ, situated between
the muscle and tendon. This detects muscle force and, if muscle force becomes excessive, the
reflex inhibits motor neurone activity. This is possible because the reflex involves an
inhibitory interneurone (a neurone that connects two other neurones) in the spinal cord.
A third reflex is the withdrawal and crossed extensor reflex. When we stand on an object that
causes pain, the reflex activates (flexor) muscles in the same leg, and inhibits (extensor)
muscles in that leg. This causes us to lift the leg off the ground. In order to support our weight
on the other leg, the other leg must be stiffened, and this is done by activating (extensor)
muscles in the other leg.
Walking involves alternation between two phases: the stance phase, which involves activation
of (extensor) muscles, and the swing phase, which involves activation of (flexor) muscles.
The part of the central nervous system that generates the walking rhythm is the spinal cord.
Four brain structures involved in movement are the motor cortex, cerebellum, brainstem and
basal ganglia. Initiating movement as well as ensuring muscle relaxation at rest are the
functions of the basal ganglia, and damage to this area results in Parkinson’s disease. The
motor cortex is responsible for generating the “motor plan” that defines the whole of a
movement, and the cerebellum receives a copy of the motor plan and compares it with
sensory information about what actually happened, in order to correct the motor plan while it
is in progress, and refine it for future occasions.